Vanadium mimics many of the actions of insulin in the body and has been studied for a potential role in the treatment of obesity, hypertension, diabetes and insulin resistance.
Vanadium is a beautifully coloured mineral which occurs in nature only in combination with other elements. Once refined, the outer layer oxidises, protecting the interior from oxidation. The photograph to the left is of refined vanadium in various states of oxidation. There are many forms of vanadium, but for therapeutic purposes vanadyl sulfate is most appropriate.
A study on human volunteers with type II diabetes found that fasting blood sugar levels and HbA1c levels dropped by around 10-15% after three weeks of therapy with 100 mg per day of vanadyl sulfate and that the effects were sustained two weeks after therapy ceased. The study found that these effects were caused by a reduction in the production of glucose by the liver and an increase in the uptake of glucose by peripheral muscle cells. 80% of the effect was attributed to increased peripheral insulin sensitivity. Like d-chiro-inositol, vanadium’s action on glucose metabolism appears to be largely post-receptor or within the cell.
It is worth noting that 75% of the participants in the study experienced some gastrointestinal distress during the first week of the study as a result of the extremely high dosage. Whilst the study did split the daily dosage amount into two separate doses, it may be beneficial to slowly build up intestinal tolerance over a week.
Long-term vanadium treatment causes marked and sustained decreases in plasma glucose, triglyceride and cholesterol levels. Chronic treatment also ameliorates secondary complications of diabetes including cardiomyopathy, vascular hyperactivity and cataract formation. There is also some evidence that it may stimulate protein synthesis and thus muscle tissue development.
Vanadium supplements at very high doses seem to improve insulin receptor sensitivity in those in whom its function is impaired. Studies indicate that therapeutic results are achieve in 50% of people at 300 mg/day.
Other studies in rats indicate that vanadium therapy has long-lasting effects, providing up to 20 weeks protection against pancreatic damage from just two weeks of treatment in 50% of subjects. This study found evidence to support the theory that vanadium has a protective effect on pancreatic beta-cells, which are responsible for producing insulin.
Like metformin, long term treatment with vanadium normalises the amount of glucose produced by the liver. When rats are treated with vanadium and then given insulin, they are more sensitive towards that insulin. I.e. the reduction in blood glucose levels is greater in the rats who received vanadium treatment, compared with controls, who did not. Vanadium treatment also restores insulin stimulated MAP and S6 kinase activities in skeletal muscle tissue. MAP stands for mitogen activated protein and they regulate various cellular activities. S6 kinase is a family of protein kinases involved in signal transduction. Some studies have used vanadium in conjunction with selenium to improve insulin sensitivity with positive results.
That vanadium compounds act in an insulin-mimetic fashion both in vitro and in vivo has been well established. Both inorganic and organic vanadium compounds have been shown to lower plasma glucose levels, increase peripheral glucose uptake, improve insulin sensitivity, decrease plasma lipid levels, and normalize liver enzyme activities in a variety of animal models of both type I and type II diabetes. Vanadium treatment of diabetic animals does not restore plasma insulin levels but may spare pancreatic insulin.
The exact cellular mechanism of action of vanadium appears to involve a combination of several post-receptor events in the insulin-signaling cascade, as is the case with d-chiro inositol. Vanadium has a broad range of effect on multiple components of carbohydrate metabolism including glucose transport, glucose transporter translocation, glycolysis and glycolytic enzymes, glucose oxidation, glucose output and glycogen synthesis. The insulin-like effects of vanadium also extend to the lipid metabolic pathways and on protein metabolism and mitogenesis. Chronic vanadium treatment corrects abnormalities in glycolytic enzymes such as phosphofructokinase-2 and glucokinase.
Whilst the research into the effect of vanadium on carbohydrate metabolism and insulin sensitivity is intriguing, it is essential to be cautious with applying this information to human therapy. At higher intakes, such as appear to be required for a therapeutic effect on carbohydrate metabolism, vanadium accumulates in body tissues such as liver, kidney and bone and symptoms of overdose may become apparent.
The average diet provides between 10-30 µg of vanadium per day. The National Academy of Sciences Food and Nutrition Board have established a maximum safe long-term daily dose of 1.8 mg. The dosages required to achieve a therapeutic effect from vanadium are clearly significantly higher than this and thus vanadium therapy for insulin resistance must be considered to fall within the orthomolecular or pharmacological range, rather than that of a nutritional supplement.
Long-term vanadium treatment causes marked and sustained decreases in plasma glucose, triglyceride and cholesterol levels, three markers which are commonly elevated in women with PCOS. Chronic treatment with vanadium also ameliorates the secondary complications of diabetes including cardiomyopathy, hypertension, vascular hyperactivity and cataract formation. As many women with PCOS progress to full-blown Type II diabetes in later life, this is a mineral which we should all consider, albeit with caution.
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